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Pharmacology > Pharmacology in Pain Management > Flashcards

Pharmacology in Pain Management Flashcards

1
Q

mild pain

A

(1-3)

-use step 1 drugs (NSAIDS & acetaminophen)

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2
Q

pain is a reflection of what?

A

emotion and attitude

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3
Q

R: region

A

where is it? does it stay there?

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4
Q

treatments

A

-2nd line:
Tryptans are serotonin/ 5-HT-1 receptors against that constrict intracranial vessels.
sumatriptans, zolmitriptan, rizatriptan, etc. (have various half-lives, times of onset)

some also come in combo, sumatriptan plus naproxin

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5
Q

tension headaches

A
  • dull quality, pain radiates to forehead, neck, shoulders
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6
Q

how do we assess pain?

A

PQRSTU

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7
Q

severe pain

A

(7-10)

-use opiates/ step 3 (morphine, hydromorphone/dilaudid, oxycodone/oxycontin, oxymorphone, Fentora)

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8
Q

Local anesthetics

A

sodium channel blockers that reduce pain impulses (novocaine)
(lidocaine)

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9
Q

transmission

A

through dorsal horn of cord; if signal is strong enough, may reach CNS, though there are inhibitory fibers in cord to reduce upstream signal

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10
Q

treatment of tension headache

A
  • acetaminophen & aspirin (1st line)
  • NSAIDS (2nd line)
    • can give antiemetics if accompanying nausea (promethazine/ prochlorperazine)
  • combination of meds: (3rd line)
  • Fioricet (butalbital/ acetaminophen/ caffeine)
  • Fiorinal (butalbital/ aspirin/ caffeine)
  • *** some anti-depressants also used, including amitriptyline, fluoxetine, others
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11
Q

chronic pain:

A
  • lasts over 3-6 months
  • pain persists after injury has healed
  • can be from a variety of tissues
  • perhaps the result of “neuroplasticity”
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12
Q

anti-convulsants

A

gabapentin & pregabalin activate GABA receptors & reduce neutotransmitters

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13
Q

acute pain

A

sudden onset & related to a specific case (trauma/damage)

  • can be accompanied by other physiological responses, (increased HR, sweating, rapid breathing)
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14
Q

Treating pain

A

mild pain
moderate pain
severe pain

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15
Q

what is pain?

A

Unpleasant sensory & emotional experience associated w/ actual or potential tissue damage

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16
Q

signal reducers

A

those that normally inhibit pain signals

-B-endorphin (mu receptors), NE, and GABA

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17
Q

what is pain pathophysiology?

A

transduction
transmission
perception
modulation

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18
Q

mediators or pain signals

A

PG’s, substance P (even stimulating second order neurons in cord)
bradykinins

19
Q

P: precipitating/ palliating

A

what makes it worse or better?

20
Q

treatments

A 
-3rd line:
Ergot derivatives (ergotamine or dihydroergotamine)
lead to vasoconstriction
21
Q

Co-Analgesics for pain

A

Antidepressants
Anticonvulsants
Local Anesthetics
Muscle Relaxants

22
Q

Migraine triggers?

A
  • physiologic factors(anxiety, depression)
  • medications (hormones, nicotine, nitroglycerin)
  • diet (alcohol, caffeine, chocolate)
  • environment (light, altitude, odors, sounds, weather)
  • lifestyle (dieting, exercise, sleep patterns)
  • hormonal factors (pregnancy, menopause)
23
Q

transduction

A

A-delta nerves and C-nerves (fibers) are activated by PGs, substance P, histamine, etc

24
Q

modulation

A

inhibitory effects in the CNS to reduce the sense of pain in a descending pathway

25
Q

moderate pain

A

(4-6)

-use NSAIDS plus opiates/ step 2 (hydrocodone/Vicodin, oxycodone/Percocet)

26
Q

S: severity

A

Pain scales?

27
Q

treatments

A

-1st line:
(NSAIDS & aspirin)
caffeine- containing meds (Excedrin (migraine))

28
Q

perception

A

signals in both the cortex and limbic system
=
COGNITIVE & EMOTIONAL component

29
Q

cluster headaches

A

disabling, burning, or boring feeling around one eye & extremely painful

30
Q

migraine

A

head throbbing, nausea, photophobia, photophobia, and can be debilitating

31
Q

Headaches

A

tension headaches
migraines
cluster headaches

32
Q

anti-depressants

A

tricyclics & SNRI will reduce NE uptake & help reduce neurotransmitters in nociception (amitriptyline & venlafaxine)

33
Q

chronic pain

A

LONG-LIVED acute pain where patients can accommodate to the physiological response
- CAN OFTEN LEAD TO DEPRESSION AND ANXIETY

34
Q

what causes migraine headaches?

A
  • can be genetic somewhat, often associated w/ LOW estrogen levels
  • thought to be vascular (too much vasodilation in cranial vessels)
    but NOW, believed to be more neurogenic, involving neurons from the trigeminal nerve leading to vasodilation of meningeal blood vessels, release of inflammatory agents, more dilation, then headache
35
Q

what causes tension headaches?

A
  • thought to be due to muscle tone in pericardial region
  • often associated with sleep deprivation, smoking, cessation
  • if treated too often, can lead to MOH (medication Overuse Headache)
36
Q

types of pain

A

nociceptive
neuropathic
acute
chronic

37
Q

Q: quality

A

what does it feel like?

38
Q

T: temporal patterns

A

is it constant? intermittent?

39
Q

Prophylaxis of migraines

A
  • 1st line: Beta blockers (propanolol, metoprolol, atenolol, etc) or tricyclic
    antidepressants (imipramine, nortriptyline, amitriptyline)

anticonvulsants (valproic acid, topiramate)
Calcium Channel Blockers

40
Q

neuropathic pain

A

from CNS processing following insult from disease or trauma such as:
tingling, burning, shooting, etc.,

41
Q

Muscle relaxants

A

likely only used when pain is related to muscle spasm

42
Q

Rescue agent?

A

opioids such as: butorphanol or codeine can be used

43
Q

U: you

A

how does it affect you?

44
Q

nociceptive pain

A

from stimulation of neurons following injury, disease of inflammation of tissue

  • can be somatic (muscle, skin, or bone associated)
  • can be visceral (organ associated)

Pharmacology (17 decks)

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